Hepcidin Levels Research Articles

Could Hepcidin Be a New Biomarker in Patients with Idiopathic Pulmonary Fibrosis (IPF)?

Objectives: Hepcidin is a biomarker produced by hepatocytes in chronic disease anemia and is known to increase during chronic inflammation. This study compares the hepcidin levels in idiopathic pulmonary fibrosis (IPF) patients and controls, evaluating its relationship with anemia and systemic inflammation in IPF patients. Methods: This study included 82 IPF patients and 31 controls. Hepcidin levels were compared between the two groups. In the IPF group, the hepcidin and anemia parameters were compared between anemic and non-anemic patients. The significance between the hepcidin and systemic inflammation parameters such as Erythrocyte Sedimentation Rate, CRP (C-reactive protein) levels, ferritin levels, and the Systemic Immune–Inflammation Index (SII) was investigated. Erythrocyte Sedimentation Rate, C-reactive protein (CRP) levels, and ferritin levels were measured using automated analyzers. Hepcidin and erythropoietin (EPO) levels were determined using ELISA kits. Results: A significant difference in hepcidin levels was found between the IPF and control groups (37.13 ± 14.92 vs. 25.77 ± 11.25, p < 0.001). No significant difference in hepcidin levels was found between anemic and non-anemic IPF patients (38.25 ± 16.2 vs. 36.7 ± 14.6, p = 0.719). No significant correlation was found between hepcidin levels and anemia parameters (serum iron, ferritin, vitamin B12, serum transferrin, transferrin saturation, total iron-binding capacity, hemoglobin, folate, and erythropoietin) in IPF patients. Despite significant differences in the systemic inflammation parameters (ferritin and CRP) between patients and controls, no significant correlation was found between their hepcidin and systemic inflammation parameters. Conclusions: Our study demonstrates that the hepcidin levels in IPF patients are elevated independently of anemia and systemic inflammation. We propose that hepcidin could be a potential biomarker to be investigated in IPF patients.

Alterations of Hepcidin and Iron Markers Associated with Obesity and Obesity-related Diabetes in Gambian Women

Aims Obesity, type 2 diabetes (T2D), and chronic inflammation are associated with disturbances in iron metabolism. Hepcidin is hypothesized to play a role in these alterations owing to its strong association with inflammation via the JAK-STAT3 pathway. The current study investigated the differences between inflammatory markers and iron indices and their association with hepcidin in lean women, women with obesity, and women with obesity and T2D (obesity-T2D) in The Gambia. Materials and methods In a cross-sectional study design, fasted blood samples were collected from three groups of women: lean women (n=42, body mass index (BMI)=20.9 kg/m2), women with obesity (n=48, BMI=33.1 kg/m2) and women with obesity-T2D (n=30, BMI=34.5 kg/m2). Markers of inflammation (IL-6 and CRP) and iron metabolism [hepcidin, iron, ferritin, soluble transferrin receptor (sTfR), transferrin, transferrin saturation, and unsaturated iron-binding capacity (UIBC)] were compared using linear regression models. Simple regression analyses were performed to assess the association between hepcidin levels and respective markers. Results Women with obesity and obesity-T2D showed elevated levels of inflammatory markers. There was no evidence that markers of iron metabolism differed between lean women and obese women, but women with obesity-T2D had higher transferrin saturation, higher serum iron concentration, and lower UIBC. Serum hepcidin concentrations were similar in all the groups. Hepcidin was not associated with markers of inflammation but was strongly associated with all other iron indices (all P<0.002). Conclusion Contrary to our original hypothesis, hepcidin was not associated with markers of inflammation in the three groups of Gambian women, despite the presence of chronic inflammation in women with obesity and obesity-T2D.

Hepcidin levels in Mexican pregnant women without family preeclampsia

Hepcidin levels in Mexican pregnant women without family preeclampsia

Obesity and iron deficiency: what is the connection and how to treat?

The article presents a review of the literature and our own data on the etiology and pathogenesis of iron deficiency and iron deficiency anemia in patients with obesity. Obesity is considered as a subclinical systemic chronic inflammation, which is associated with an increase in the level of hepcidin, which is a key mediator of anemia during inflammation. Patients with obesity should undergo periodic screening of iron status and ferrokinetic parameters. Today, new oral iron preparations with increased tolerability and improved absorption are used in clinical practice. These include sucrosomial iron preparations. Sucrosomial iron (SI) is an innovative oral iron-containing carrier in which iron pyrophosphate is enclosed in a phospholipid matrix coated with sucrester, which protects sucrosomial iron from the effects of gastric juice, excluding contact with the mucous membrane of the gastrointestinal tract. Resistance to the action of gastric juice allows intact sucrosomes to reach the mucous membrane of the small intestine, where they are absorbed through special M cells, followed by the release of iron in liver cells. This allows prescribing SI to patients with iron deficiency and inflammatory bowel diseases, celiac disease, cancer and patients with obesity. Sucrosomial iron should be considered as an alternative treatment for iron deficiency in obese women. SI is innovative, allowing to bypass the “hepcidin barrier”, convenient for administration, effective for treatment, well tolerated than traditional oral iron salts.

Influence of TMPRSS6 genotype on iron status parameters in stable COPD patients

Background: The SNP rs855791 has been linked to increased hepcidin levels, variations in serum iron, transferrin saturation and red blood cell indices. Our goal was to determine the prevalence of this polymorphism among COPD patients and to assess its impact on iron status parameters including hepcidin in patients with stable COPD. Methods: We analysed iron status parameters and genetic data form 94 COPD patient: 29 patients with wild-type genotype (WT group) and 65 patients with either homozygous or heterozygous genotype (HH group). Additionally, the prevalence of SNP rs855791 was assessed in 192 volunteers. Results: The frequency distribution of SNP rs855791 was comparable between the COPD patients and control subjects (p=0.791). Iron status parameters were within their respective reference values and did not show neither statistically nor clinically significant difference between the WT and HH group of COPD patients. However, after excluding patients with (sub)clinical vitamin B12 deficiency and/or hypoxemia, WT group of patients exhibited significantly lower erythropoietin levels (p=0.015). The area under the curve for EPO was 0.688 (95% CI: 0.545-0.830, p=0.015), with an optimal cut-off of 9.74, sensitivity of 61.2% (95% CI: 58.1-64.3) and specificity of 65.0% (95% CI: 61.8-68.3). Conclusion: In patients with stable COPD, iron status parameters do not differ between WT and HH group of patients. After excluding those with (sub)clinical vitamin B12 deficiency and/or hypoxia, only statistical and not clinical difference in EPO levels was observed suggesting that EPO may regulate hepcidin levels and thus influence the development of iron deficiency and/or anaemia.

Effect of dietary protein on serum hepcidin and iron in adults with obesity and insulin resistance: A randomized single blind clinical trial.

Background and AimsBoth obesity and iron deficiency are public health problems. The association between the two problems could be explained by chronic low-grade inflammation in obesity, which could stimulate hepcidin expression and modify iron concentration that the consumption of high-protein diets could prevent. Thus, this study aimed to compare the effects of high-protein diets with a predominance of animal or vegetable protein on serum hepcidin and iron concentrations in adults with obesity. Methods and ResultsThis randomized clinical trial involved adults with obesity and insulin resistance, who were assigned to either a high animal protein (AP) group or a high vegetable protein (VP) group for a one-month intervention. Both groups followed a calorie-restricted diet, reducing energy intake by 750 kcal/day. Baseline and final measurements included serum concentrations of hepcidin and iron, biochemical parameters, anthropometric data, and body composition. A total of 33 participants (63% female) were included in the study. Significant weight loss was observed in both groups after the intervention. Adjusted for weight loss percentage, the AP group showed a significant increase in hepcidin concentration (from 22.3 ± 14.7 to 27.5 ± 19.5 ng/mL) compared to the VP group (from 17.9 ± 15.1 to 17.2 ± 10.1 ng/mL) (p < 0.01), with no changes in serum iron concentration. Additionally, the VP diet significantly reduced serum adiponectin (p = 0.04) and C-reactive protein (p = 0.03) levels. ConclusionsIn adults with obesity following the AP diet for one month, hepcidin levels increased without affecting serum iron concentrations. Trial registrationNCT03627104

Inflammatory biomarkers and hepcidin levels in Iron deficiency anemia among women of reproductive age

Inflammatory biomarkers and hepcidin levels in Iron deficiency anemia among women of reproductive age

The Relationship Between Ghrelin and Iron Metabolism In Beta Thalassemia Major Patients

IntroductionStudies in beta thalassemia major (β-TM) patients have shown that the responses of HIF2α, hepcidin and ferroportin molecules to high iron levels are impaired. In recent years, studies conducted in patients with iron deficiency anemia have investigated the relationship between ghrelin hormone and iron metabolism. In this study, we aimed to contribute to the etiopathogenesis of this disease by examining the changes in ghrelin hormone levels in patients with β-TM.Material and methodsFifty-two β-TM and 23 controls were included in our study. Blood counts, routine biochemical parameters, HIF2α, hepcidin and ghrelin levels were studied in blood samples taken from the volunteers.ResultsErythrocyte indexes, serum bilirubin, iron, unsaturated iron binding capacity, total iron binding capacity and ferritin levels showed significant differences between two groups (p&lt;0.05) . There was no significant difference between two groups for serum HIF2α and hepcidin levels. When two groups were compared, ghrelin levels were found to be significantly higher in patients (p&lt;0.05). When the correlation between parameters was examined in all subjects, a weak positive correlation was found between ghrelin and HIF2α (r=0.263) (p&lt;0.05) and a significant positive correlation was found between ghrelin and ferritin (r=0.417) (p&lt;0.05).ConclusionsOur study showed that there is a positive correlation between ghrelin and ferritin levels. Elevated ghrelin levels in patients with β-TM may have an important role in regulating impaired iron metabolism. Molecular level studies are needed to determine synthesis pathways.

Hepcidin, GDF-15 and their Impact on Iron Metabolism in CKD

Background Anemia is an important complication in chronic kidney disease (CKD). We studied the diagnostic accuracy of hepcidin and growth differentiation factor-15 (GDF-15) as early markers of iron deficiency anemia (IDA) in non-dialysis (ND-CKD) patients. Materials and Methods This was a cross-sectional, case-control study comprising 100 cases of CKD (newly diagnosed and non-dialyzed) and 40 healthy controls. Serum levels of hepcidin and GDF-15 were estimated using ELISA-based assays. Receiver operator characteristics were used to evaluate the diagnostic validity of hepcidin and GDF-15 for absolute and functional iron deficiency anemia. Results About 33% of the cases were females with a mean age of 47.64 (± 13.68) years. The predictive value of hepcidin for diagnosing functional IDA in CKD was found to be 69.1% (95% CI: 52.5% to 82.7%), and that of GDF-15 was found to be 68.8% (95% CI: 52.6% to 82.1%). Hepcidin significantly correlated with hemoglobin (r = 0.278, p = 0.005) and serum iron (r = 0.222; p = 0.025). GDF-15 positively correlated with ferritin (r = 0.346, p &lt; 0.0001) and hsCRP (r = 0.223, p = 0.0088) and negatively correlated with eGFR (r = -0.462, p &lt; 000001), Hb (r = -0.481, p &lt; 0.00001) and TIBC (r = -0.353, p &lt; 0.0001). Conclusion Hepcidin and GDF-15 could predict functional IDA in our patients but not absolute IDA.

The hepcidin-ferroportin axis modulates liver endothelial cell BMP expression to influence iron homeostasis in mice

The liver hormone hepcidin regulates systemic iron homeostasis to provide enough iron for vital processes while limiting toxicity. Hepcidin acts by degrading its receptor ferroportin (encoded by Slc40a1) to decrease iron export to plasma. Iron controls hepcidin production in part by inducing liver endothelial cells (LECs) to produce bone morphogenetic proteins (BMPs), which activate hepcidin transcription in hepatocytes. Here, we used in vitro and in vivo models to investigate whether ferroportin contributes to LEC intracellular iron content to modulate BMP expression and thereby hepcidin. Quantitative proteomics of LECs from mice fed different iron diets demonstrated an inverse relationship between dietary iron and endothelial ferroportin expression. Slc40a1 knockdown primary mouse LECs and endothelial Slc40a1 knockout mice exhibited increased LEC iron and BMP ligand expression. Endothelial Slc40a1 knockout mice also exhibited altered systemic iron homeostasis with decreased serum and total liver iron but preserved erythropoiesis. Although endothelial Slc40a1 knockout mice had similar hepcidin expression as control mice, hepcidin levels were inappropriately high relative to iron levels. Moreover, when iron levels were equalized with iron treatment, hepcidin levels were higher in endothelial Slc40a1 knockout mice than controls. Finally, LEC ferroportin levels were inversely correlated with hepcidin levels in multiple mouse models, and treatment of hepcidin-deficient mice with mini-hepcidin decreased LEC ferroportin expression. Overall, these data show that LEC ferroportin modulates LEC iron and consequently BMP expression to influence hepcidin production. Furthermore, LEC ferroportin expression is regulated by hepcidin, demonstrating bidirectional communication between LECs and hepatocytes to orchestrate systemic iron homeostasis.

Preterm Piglets Born by Cesarean Section as a Suitable Animal Model for the Study of Iron Metabolism in Premature Infants.

Preterm infants are most at risk of iron deficiency. However, our knowledge of the regulation of iron homeostasis in preterm infants is poor. The main goal of our research was to develop and validate an animal model of human prematurity to assess iron status in preterm infants. We performed a cesarean section on sows on the 109th day of pregnancy, which corresponds to the last trimester of human pregnancy. Preterm piglets showed decreased body weight, red blood cell indices, plasma iron level and transferrin saturation. Interestingly, higher hepatic and splenic non-heme iron content and plasma and hepatic ferritin levels were found in premature piglets compared with term ones. In addition, premature piglets showed higher mRNA levels of iron-regulatory hormone hepcidin in the liver than term animals, which have not been reflected in higher plasma hepcidin-25 levels. We also showed changes in hepcidin regulators, including hepatic bone morphogenetic protein 6, plasma erythroferrone and growth differentiation factor 15 in preterm piglets. Consequently, no difference was observed in iron-exporter ferroportin levels in the spleen and liver. Overall, it seems that premature piglets show a pattern of iron metabolism characteristic of functional iron deficiency and iron accumulation in the tissue.

A novel synthetic compound, deferiprone–resveratrol hybrid (DFP-RVT), promotes hepatoprotective effects and ameliorates iron-induced oxidative stress in iron-overloaded β-thalassemic mice

A high amount of iron in β-thalassemia patients can lead to oxidative stress and organ dysfunction, especially liver, the main iron accumulated organ. Iron catabolism causes the generation of reactive oxygen species (ROS), triggering liver inflammation, fibrosis, and cirrhosis. Deferiprone-resveratrol hybrid (DFP-RVT) is chemically synthesized by combining deferiprone (DFP) and resveratrol (RVT) which shows an iron-chelating property along with antioxidant activity. This study explored the hepatoprotective effect of DFP-RVT in iron overloaded β-knockout (BKO) thalassemic mice. The results revealed that DFP-RVT treatment improved liver function in iron-overloaded BKO mice by reducing liver enzymes and increasing hepcidin levels compared to iron overload control mice. Both DFP alone and DFP-RVT treatment groups demonstrated iron chelation effects by decreasing liver iron content (LIC), iron profiles, and iron deposition in the liver. Moreover, DFP-RVT powerfully showed antioxidant properties by decreasing liver and plasma thiobarbituric acid reactive substances (TBARs) and increasing reduced glutathione (GSH) and superoxide dismutase (SOD). Interestingly, transforming growth factor β1 (TGFβ1), which can contribute to chronic liver disease through liver injury, inflammation, fibrosis, and cirrhosis, is highly expressed in iron-overloaded mice. However, both DFP and DFP-RVT treatment significantly reduced TGFβ1 levels compared to the iron-overloaded group. Therefore, DFP-RVT could be a potent hepatoprotective compound through the mobilization of iron, reduction of ROS, improvement of liver enzymes, and alleviation of liver damage, potentially relieving liver dysfunction in iron-overloaded BKO mice.

Predictive value of serum hepcidin levels for the risk of incident end-stage kidney disease in patients with chronic kidney disease: The KNOW-CKD

Introduction: Despite the pivotal role of hepcidin in the development of anemia among the patients with chronic kidney disease (CKD), the association between serum hepcidin levels and CKD progression has been never investigated. We here hypothesized that elevation in serum hepcidin levels might be associated with the risk of incident end-stage kidney disease (ESKD) among the patients with pre-dialysis CKD. Methods: A total of 2,109 patients with pre-dialysis CKD at stages 1 to pre-dialysis 5 were categorized into the quartiles by serum hepcidin levels. The study outcome was incident ESKD. The median duration of follow-up was 7.9 years. Results: The analysis of the baseline characteristics revealed that unfavorable clinical features were in general associated with higher serum hepcidin levels. The cumulative incidence of ESKD was significantly differed by serum hepcidin levels, with the highest incidence in the 4th quartile (P &lt; 0.001, by log-rank test). Cox regression analysis demonstrated that, compared to the 1st quartile, the risk of incident ESKD is significantly increased in the 4th quartile (adjusted hazard ratio 1.372, 95% confidence interval 1.070 to 1.759). Penalized spline curve analysis illustrated a linear, positive correlation between serum hepcidin levels and the risk of incident ESKD. Subgroup analyses revealed that the association is significantly more prominent in the patients with advanced CKD (i.e., estimated glomerular filtration rate &lt; 45 mL/min/1.73 m2). Conclusion: Elevation in serum hepcidin levels is significantly associated with the risk of incident ESKD among the patients with pre-dialysis CKD.

Hepcidin levels, markers of iron overload, and liver damage in children with beta-thalassemia major

Background Thalassemia is a hemoglobin synthesis disorder that causes patients to need lifelong blood transfusions, leading to iron overload and alter organ function, including the liver. Hepcidin, produced by the liver, plays a role in iron homeostasis and should be increased in excess iron stores. However, the level decreases in thalassemia due to some factors, such as ineffective erythropoiesis and liver damage. Recent publications revealed that hepcidin could be associated with iron overload and also a marker of liver diseases. Objective To analyse the correlation between hepcidin level, markers of iron overload, and liver damage in beta-thalassemia major. Methods This cross-sectional study included all ?-thalassemia major age 2-18 years admitted to Dr. Mohammad Hoesin Hospital, Palembang, South Sumatera, who underwent blood transfusions from March to August 2022. We measured the level of iron overload markers, hepcidin, liver function test (LFT), and performed liver ultrasonography (USG). Results Of 97 subjects, median hepcidin level was 10.01 ng/mL and 68% of the subjects showed a decrease. The iron overload parameters were evaluated from serum iron levels (P=0.13), ferritin levels (P=0.90), and transferrin saturation (P=0.29) and 24.7% had abnormal liver USG findings. Spearman’s correlation revealed that only direct bilirubin (DB) (r=0.35; P=0.001) and liver USG (r=0.20; P=0.05) had positive correlations with decreased levels of hepcidin. Also, it had 91.7% sensitivity in predicting liver damage from ultrasound. Conclusion The hepcidin level was not significantly associated with iron overload markers.

Serum Levels of the C-terminal Fragment of Fibroblast Growth Factor 23 (C-FGF23) and Hepcidin in Patients with Hemodialysis Undergoing Treatment with a Proline Hydroxylase Domain (PHD) Inhibitor

Background: We previously reported, for the first time, serum levels of the C-terminal fragment of fibroblast growth factor 23 (C-FGF23) in patients undergoing hemodialysis (HD). Most HD patients have undergone treatment with either recombinant erythropoietin (r-EPO) or hypoxia-inducible factor (HIF) proline hydroxylase domain (PHD) inhibitor, both of which stimulate FGF23 production and cleavage. Methods: This cross-sectional observational study involved analyzing measuring FGF-related parameters and comparing results for subgroups of patients who received either r-EPO and or a PHD inhibitor. Results: No significant difference was observed for iron-related parameters or serum hepcidin levels in both subgroups of patients. Significant differences were found for certain FGF-23-related parameters. Conclusion: Both FGF23 production and cleavage were stimulated more in patients treated with the PHD inhibitor than in patients treated with r-EPO.

Hepatocyte activation and liver injury following cerebral ischemia promote HMGB1-mediated hepcidin upregulation in hepatocytes and regulation of systemic iron levels

We previously reported that high mobility group box 1 (HMGB1), a danger-associated molecular pattern (DAMP), increases intracellular iron levels in the postischemic brain by upregulating hepcidin, a key regulator of iron homeostasis, triggering ferroptosis. Since hepatocytes are the primary cells that produce hepcidin and control systemic iron levels, we investigated whether cerebral ischemia induces hepcidin upregulation in hepatocytes. Following middle cerebral artery occlusion (MCAO) in a rodent model, significant liver injury was observed. This injury was evidenced by significantly elevated Eckhoff’s scores and increased serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Additionally, total iron levels were significantly elevated in the liver, with intracellular iron accumulation detected in hepatocytes. Hepcidin expression in the liver, which is primarily localized in hepatocytes, increased significantly starting at 3 h after MCAO and continued to increase rapidly, reaching a peak at 24 h. Interestingly, HMGB1 levels in the liver were also significantly elevated after MCAO, with the disulfide form of HMGB1 being the major subtype. In vitro experiments using AML12 hepatocytes showed that recombinant disulfide HMGB1 significantly upregulated hepcidin expression in a Toll-like receptor 4 (TLR4)- and RAGE-dependent manner. Furthermore, treatment with a ROS scavenger and a peptide HMGB1 antagonist revealed that both ROS generation and HMGB1 induction contributed to hepatocyte activation and liver damage following MCAO–reperfusion. In conclusion, this study revealed that cerebral ischemia triggers hepatocyte activation and liver injury. HMGB1 potently induces hepcidin not only in the brain but also in the liver, thereby influencing systemic iron homeostasis following ischemic stroke.

GBT1118, a Voxelotor Analog, Ameliorates Hepatopathy in Sickle Cell Disease.

Background and Objectives: In sickle cell disease (SCD), hepatopathy is a cumulative consequence of ischemia/reperfusion (I/R) injury from a vaso-occlusive crisis, tissue inflammation, and iron overload due to blood transfusion. Hepatopathy is a major contributing factor of shortened life span in SCD patients. We hypothesized that the voxelotor, a hemoglobin allosteric modifier, ameliorates sickle hepatopathy. Materials and Methods: Townes SCD mice and their controls were treated with either chow containing GBT1118, a voxelotor analog, or normal chow. We evaluated inflammation, fibrosis, apoptosis and ferroptosis in their livers using qPCR, ELISA, histology, and immunohistochemistry. Results: GBT1118 treatment resulted in reduced hemolysis, iron overload and inflammation in the liver of SCD mice. There were significant reductions in the liver enzyme levels and bile acids. Furthermore, GBT1118-treated mice exhibited reduced apoptosis, necrosis, and fibrosis. Increased ferroptosis as evident from elevated 4-hydroxynonenal (4-HNE) staining, malondialdehyde (MDA) levels, and expression of Ptgs2 and Slc7a11 mRNAs, were also significantly reduced after GBT1118 treatment. To explain the increased ferroptosis, we evaluated iron homeostasis markers in livers. SCD mice showed decreased expression of heme oxygenase-1, ferritin, hepcidin, and ferroportin mRNA levels. GBT1118 treatment significantly increased expressions of these genes. Conclusions: Our results suggest GBT1118 treatment in SCD confers the amelioration of sickle hepatopathy by reducing inflammation, fibrosis, apoptosis, iron overload and ferroptosis.

Iron Deficiency and its Relationship with Chronic Heart Failure- A Review.

This review article discusses multifactorial pathophysiology, the relationship between clinical characteristics, functional and absolute ID, and the advantages of medicinal intervention in chronic heart failure (CHF). It also covers how iron shortage affects other body parts. The most recent publications that included substantial scientific data on the connection between CHF and ID, with or without anaemia, were selected. Complex physiopathological interactions, including higher hepcidin levels, systemic inflammation, and activation of the renin-angiotensin-aldosterone system, have been identified in these patients. These mechanisms exacerbate the outcomes for patients by amplifying the severity of anemia, chronic heart failure (CHF), and Chronic kidney disease (CKD). Research in this area has been limited and has shown inconsistent findings. Still, it has also examined evidence-based treatment approaches and diagnostic guidelines, especially in relation to iron supplements and erythropoietin-stimulating medications. Anemia is a frequent chronic heart failure consequence and a poor prognostic factor. We still don't completely understand the many complex causes of anemia. Iron deficiency screening is highly recommended for people with cardiac ailments because of its significance for their prognoses. Due to the paucity of research proving its effectiveness, the high incidence of unfavourable gastrointestinal side effects, and the prolonged length of time required for treatment to boost haemoglobin levels, an oral iron supplement is not advised for people with chronic heart failure. An insufficient amount of iron not only impacts the heart but also various other body components.

Intact FGF23 and Markers of Iron Homeostasis, Inflammation, and Bone Mineral Metabolism in Acute Pediatric Infections.

We intend to evaluate the association of intact Fibroblast Growth Factor 23 (i-FGF23), a phosphaturic hormone that contributes to anemia of inflammation, with markers of iron homeostasis, inflammation, and bone mineral metabolism in acute pediatric infections. Seventy-nine children, aged 1 month-13 years, out of which forty-two were males and thirty-seven females, participated in this study. Children with diseases and nutrient deficiencies causing anemia were excluded. Twenty-six patients had bacterial infections, twenty-six had viral infections, and twenty-seven children served as healthy controls. Complete blood count, markers of inflammation, iron and mineral metabolism, serum hepcidin, and i-FGF23 were compared between the groups. Thirty-nine percent of patients with bacterial infection and twelve percent of patients with viral infection presented characteristics of anemia of inflammation (p < 0.001). Ninety-two percent of patients with bacterial infection and eighty-one percent of patients with viral infection had functional iron deficiency (p < 0.001). Hepcidin was significantly positively correlated with the duration of fever, markers of inflammation, and negatively with iron, mineral metabolism parameters, and i-FGF23. i-FGF23 was positively correlated with iron metabolism parameters and negatively with the duration of fever, markers of inflammation, and hepcidin. Hepcidin levels increase, whereas i-FGF23 levels decrease in acute pediatric infections. Further research is required to understand the role of FGF23 in the hepcidin-ferroportin axis and for hepcidin in the diagnosis of bacterial infections and mineral metabolism.

Metabolic and Inflammatory Aspects of Iron Deficiency in Obese

Obesity is a chronic disease with a complex etiology, characterized by a persistent inflammatory state induced by various pro-inflammatory cytokines, including interleukin-6. This condition leads to increased production of hepcidin, a protein hormone responsible for regulating iron homeostasis. Hepcidin's primary function is to inhibit iron absorption by enterocytes, the cells lining the small intestine. Symptoms of iron deficiency, which is crucial for oxygen transport, energy production, and immune system support, can be varied and often nonspecific, such as general weakness, pallor, or concentration difficulties, potentially prolonging the diagnostic process. This article aims to analyze the relationship between obesity and iron deficiency in the metabolic context. Obesity, being one of the most prevalent health issues of the modern world, is associated with numerous complications, including disturbances in iron metabolism. Iron deficiency in obese individuals can lead to anemia, reduced physical performance, and cognitive impairments. Traditional treatment methods for this micronutrient deficiency involve supplementation. However, supplementation shows reduced efficacy in overweight and obese individuals, likely due to elevated hepcidin levels. A more effective approach should include interventions targeting not only the supplementation of the missing micronutrient but also weight reduction.